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Reactive amyloidosis and the acute phase response. bail-li┬йre's clinical rheumatology. vol. 8 no. 3

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LETTERS
Nikkari S, Mertsola J, Korvenranta H, Vainionpaa R, Toivanen
P: Wegener’s granulomatosis and parvovirus B 19 infection.
Arthritis Rheum 37:1707-1708, 1994
Corman LC, Dolson DJ: Parvovirus B19 and necrotizing vasculitis (abstract). Arthritis Rheum 35 (suppl 9):S165, 1992
Schwarz TF, Roggendorf M, Deinhardt F: Human parvovirus
B19: ELISA and immunoblot assays. J Virol Methods 20:155168, 1988
Anderson LJ, Tsou C, Parker RA, Chorba TL, WulE H, Tattersall P, Mortimer PP: Detection of antibodies and antigens of
human parvovirus B 19 by enzyme-linked immunosorbent assay.
J Clin Microbiol 24522-526, 1986
Reply
To the Editor:
Drs. Corman and Staud describe 2 patients, in addition to the 2 described previously (1,2), whose cases suggest
an association between parvovirus B 19 infection and WG.
Since our initial case (2), we have studied sera from 42 adult
patients with recent-onset WG (23 male, 19 female; ages
18-79 years). Primers specific for DNA sequences from 2
different segments of the B19 genome were used (2); primers
that amplify positions 2060-2369 were used in the sera of all
42 patients and those that amplify positions 3365-3564 were
used in the sera of 36 patients. The polymerase chain
reaction (PCR) products were further studied by Southern
hybridization using BlPspecific oligonucleotide probes.
Strict measures were taken to avoid false-positive results in
the PCR assay, usually caused by amplicon contamination of
the PCR reagents. Consecutive serum samples were available from 13 patients; from these samples, B19-specific
circulating IgM and IgG antibodies were determined using an
enzyme-linked immunosorbent assay with a recombinant
antigen (Progen, Heidelberg, Germany).
Molecular or serologic evidence of recent B 19 infection was not observed in any of these adult patients. An
explanation for our negative findings might be the age
distribution of the patients; the previously described WG
patients who were found to be B19 positive by PCR were 12
and 16 years old (1,2). Yet, Drs. Corman and Staud’s finding
of 2 adult patients with serologic evidence of B19 infection
and WG further complicates the final evaluation. However,
1175
on the basis of our present findings, we prefer to conclude
that no clear evidence exists for a B19 etiology of WG. It
should also be mentioned that suggestions about the association of B19 infection with Kawasaki disease (3) or polyarteritis nodosa (1,4) have appeared inconclusive (5,6).
Simo Nikkari, MD
Raija Vainionpaa, PhD
Paavo Toivanen, MD
Turku University
Turku, Finland
Wolfgang L. Gross, MD
Nouhad Mistry, MD
Elena Csernok, PhD
Medical University of Lubeck, Lubeck
and Rheumaklinik Bad Bramstedt
Bad Bramstedt, Germany
Wladimir Szpirt, MD
Rigshospitalet
Copenhagen, Denmark
Bo Baslund, MD
Allan Wiik, MD
Statens Seruminstitut
Copenhagen, Denmark
1. Finkel TH, Torok TJ, Ferguson PJ, Durigon EL, Zaki SR, Leung
DYM, Harbeck RJ, Gelfand EW, Saulsbury FT, Hollister JR,
Anderson LJ: Chronic parvovirus B19 infection and systemic
necrotising vasculitis: opportunistic infection or aetiological
agent? Lancet 343:1255-1260, 1994
2. Nikkari S, Mertsola J, Korvenranta H, Vainionpaa R, Toivanen
P: Wegener’s granulomatosis and parvovirus B 19 infection.
Arthritis Rheum 37: 1707-1708, 1994
3. Nigro G, Zerbini M, Krzysztofiak GG, Porcaro MA, Mango T,
Musiani M: Active or recent parvovirus B19 infection in children
with Kawasaki disease. Lancet 343: 1260-1261, 1994
4. Corman LC, Dolson DJ: Polyarteritis nodosa and parvovirus B19
infection. Lancet 339:491, 1992
5. Yoto Y, Kudoh T, Haseyama K, Suzuki N, Chiba S, Matsunaga
Y: Human parvovirus B19 infection in Kawasaki disease. Lancet
344:58-59, 1994
6. Leruez-Ville M, LaugC A, Morinet F, Guillevin L, DCny P:
Polyarteritis nodosa and parvovirus B19. Lancet 344:263-264,
1994
BOOK REVIEW
Reactive Amyloidosis and the Acute Phase Response. Bailliere’s Clinical Rheumatology. Vol. 8, No. 3. Edited by
Gunnar Husby. London, Baillizre Tindall, 19%. 200 p p .
Illustrated. Indexed. $40.00,
The acute-phase response and its role in the production of the reactive or secondary (AA) type of amyloidosis is
an exceedingly complex topic. The association was first
recognized in the early 1970s, and the mechanism appeared
simple: arthritis and other forms of inflammation produced
interleukin-1, which caused an acute-phase response and an
elevated level of serum amyloid A (SAA) protein, which in
turn led to AA amyloidosis. Now the acute-phase response
is known to be regulated by many cytokines, each with
separately regulated gene expression, and SAA is known to
be a whole family of proteins.
Research on the acute-phase response has become a
fast-paced field, with the discovery of numerous cytokines
1176
leading to a multitude of physiologic changes, one of which
is AA amyloidosis. This 11-chapter multiauthored monograph brings together a rich assortment of topics related to
reactive amyloidosis, presented by outstanding investigators
in the US, Canada, and Europe. The first chapter, by the
editor, defines the classification of amyloidosis, a topic for
which he is internationally recognized. The book then proceeds to address, in an orderly manner, the acute-phase
response, SAA protein, other constituents of connective
tissue which may influence amyloid deposition, and clinical
aspects of amyloidosis.
The first half of the book is outstanding! The chapter
on the general aspects of the acute-phase response is a
comprehensive review of inflammation as a complex, highly
orchestrated process involving many cell types and molecules. It describes the acute-phase response and the role of
cytokines as an integrated sum of multiple, separately regulated changes in gene expression. It contains an excellent list
of up-to-date references, as is also found in most of the other
chapters. The chapter on SAA as an apolipoprotein and
precursor of reactive amyloidosis discusses its regulation
and presents a complete review of SAA in all species.
Another first-rate chapter is one that reviews the components that are universally present in amyloid substance but
are not the integral elements of the fibrils: namely, P
component, apolipoprotein E, basement membrane, proteoglycans, and glycosaminoglycans. Although some overlap in
content is found in these chapters, they are presented from
different perspectives and are generally complementary.
BOOK REVIEW
The last 4 chapters address clinical aspects of amyloidosis. A chapter on epidemiology has the best information
available on the incidence of the AL (primary) type of
amyloidosis and reveals how little information there is on
this topic. Two other chapters provide incidence figures for
AA amyloidosis in different countries and discuss the variations found due to disparate underlying diseases. They
point out large differences, with a rather high prevalence of
AA amyloidosis in western Europe and a lower prevalence
in the US. A chapter on the diagnosis of amyloidosis is a
disappointingly biased review which highlights the SAP
scintigraphy test and undermines the “gold standard” of
tissue biopsy. The value of SAP scintigraphy is as yet
unconfirmed since its use is restricted to the investigators’
laboratory.
This 200-page issue of Baillitre’s Clinical Rheumatology will be most valuable for its detailed review of the
acute-phase response. Investigators in fields of inflammation
will appreciate the comprehensive and well-referenced chapters on this topic. The chapters on the clinical aspects of
reactive amyloidosis will be of great interest and value to
clinicians who study amyloid disease, but of limited value to
the practicing rheumatologist.
Martha Skinner, MD
Boston University School of Medicine
Boston, MA
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